Measurement of the electron's electric dipole moment using YbF molecules: methods and data analysis

We recently reported a new measurement of the electron's electric dipole moment using YbF molecules [Nature 473, 493 (2011)]. Here, we give a more detailed description of the methods used to make this measurement, along with a fuller analysis of the data. We show how our methods isolate the electric dipole moment from imperfections in the experiment that might mimic it. We describe the systematic errors that we discovered, and the small corrections that we made to account for these. By making a set of additional measurements with greatly exaggerated experimental imperfections, we find upper bounds on possible uncorrected systematic errors which we use to determine the systematic uncertainty in the measurement. We also calculate the size of some systematic effects that have been important in previous electric dipole moment measurements, such as the motional magnetic field effect and the geometric phase, and show them to be negligibly small in the present experiment. Our result is consistent with an electric dipole moment of zero, so we provide upper bounds to its size at various confidence levels. Finally, we review the prospects for future improvements in the precision of the experiment.Comment: 35 pages, 15 figure

Franck-Condon Factors and Radiative Lifetime of the A^{2}\Pi_{1/2} - X^{2}\Sigma^{+} Transition of Ytterbium Monoflouride, YbF

The fluorescence spectrum resulting from laser excitation of the A^{2}\Pi_{1/2} - X^{2}\Sigma^{+} (0,0) band of ytterbium monofluoride, YbF, has been recorded and analyzed to determine the Franck-Condon factors. The measured values are compared with those predicted from Rydberg-Klein-Rees (RKR) potential energy curves. From the fluorescence decay curve the radiative lifetime of the A^{2}\Pi_{1/2} state is measured to be 28\pm2 ns, and the corresponding transition dipole moment is 4.39\pm0.16 D. The implications for laser cooling YbF are discussed.Comment: 5 pages, 5 figure

Finite Volume Kolmogorov-Johnson-Mehl-Avrami Theory

We study Kolmogorov-Johnson-Mehl-Avrami (KJMA) theory of phase conversion in finite volumes. For the conversion time we find the relationship $\tau_{\rm con} = \tau_{\rm nu} [1+f_d(q)]$. Here $d$ is the space dimension, $\tau_{\rm nu}$ the nucleation time in the volume $V$, and $f_d(q)$ a scaling function. Its dimensionless argument is $q=\tau_{\rm ex}/ \tau_{\rm nu}$, where $\tau_{\rm ex}$ is an expansion time, defined to be proportional to the diameter of the volume divided by expansion speed. We calculate $f_d(q)$ in one, two and three dimensions. The often considered limits of phase conversion via either nucleation or spinodal decomposition are found to be volume-size dependent concepts, governed by simple power laws for $f_d(q)$.Comment: 4 pages, 4 figures. Additions after referee reports: Scaling of the variable q is proven. Additional references are adde

Healthcare practitioners' views and experiences of barriers and facilitators to weight management interventions for adults with intellectual disabilities

Background Obesity is common in adults with intellectual disabilities, yet little is known about how weight management interventions are provided for this population. Methods Semi‐structured interviews were held with 14 healthcare practitioners involved in weight management interventions in an English county. A study topic guide was developed to elicit practitioners' views and experiences of barriers and facilitators to weight management for adults with intellectual disabilities. Responses were analysed using thematic analysis. Results Several barriers are involved in weight management for people with intellectual disabilities including communication challenges, general practitioners' lack of knowledge and awareness of weight management services, inconsistencies in caring support, resource constraints, wider external circumstances surrounding the individuals and motivational issues. Facilitators include reasonable adjustments to existing weight management services. However, there is a need for specialist weight management provision for people with intellectual disabilities. Conclusions This study provides suggestions for future research, policy and practice consideration

Spatial Stereoresolution for Depth Corrugations May Be Set in Primary Visual Cortex

Stereo “3D” depth perception requires the visual system to extract binocular disparities between the two eyes' images. Several current models of this process, based on the known physiology of primary visual cortex (V1), do this by computing a piecewise-frontoparallel local cross-correlation between the left and right eye's images. The size of the “window” within which detectors examine the local cross-correlation corresponds to the receptive field size of V1 neurons. This basic model has successfully captured many aspects of human depth perception. In particular, it accounts for the low human stereoresolution for sinusoidal depth corrugations, suggesting that the limit on stereoresolution may be set in primary visual cortex. An important feature of the model, reflecting a key property of V1 neurons, is that the initial disparity encoding is performed by detectors tuned to locally uniform patches of disparity. Such detectors respond better to square-wave depth corrugations, since these are locally flat, than to sinusoidal corrugations which are slanted almost everywhere. Consequently, for any given window size, current models predict better performance for square-wave disparity corrugations than for sine-wave corrugations at high amplitudes. We have recently shown that this prediction is not borne out: humans perform no better with square-wave than with sine-wave corrugations, even at high amplitudes. The failure of this prediction raised the question of whether stereoresolution may actually be set at later stages of cortical processing, perhaps involving neurons tuned to disparity slant or curvature. Here we extend the local cross-correlation model to include existing physiological and psychophysical evidence indicating that larger disparities are detected by neurons with larger receptive fields (a size/disparity correlation). We show that this simple modification succeeds in reconciling the model with human results, confirming that stereoresolution for disparity gratings may indeed be limited by the size of receptive fields in primary visual cortex

Civil conflict and sleeping sickness in Africa in general and Uganda in particular

Conflict and war have long been recognized as determinants of infectious disease risk. Re-emergence of epidemic sleeping sickness in sub-Saharan Africa since the 1970s has coincided with extensive civil conflict in affected regions. Sleeping sickness incidence has placed increasing pressure on the health resources of countries already burdened by malaria, HIV/AIDS, and tuberculosis. In areas of Sudan, the Democratic Republic of the Congo, and Angola, sleeping sickness occurs in epidemic proportions, and is the first or second greatest cause of mortality in some areas, ahead of HIV/AIDS. In Uganda, there is evidence of increasing spread and establishment of new foci in central districts. Conflict is an important determinant of sleeping sickness outbreaks, and has contributed to disease resurgence. This paper presents a review and characterization of the processes by which conflict has contributed to the occurrence of sleeping sickness in Africa. Conflict contributes to disease risk by affecting the transmission potential of sleeping sickness via economic impacts, degradation of health systems and services, internal displacement of populations, regional insecurity, and reduced access for humanitarian support. Particular focus is given to the case of sleeping sickness in south-eastern Uganda, where incidence increase is expected to continue. Disease intervention is constrained in regions with high insecurity; in these areas, political stabilization, localized deployment of health resources, increased administrative integration and national capacity are required to mitigate incidence. Conflict-related variables should be explicitly integrated into risk mapping and prioritization of targeted sleeping sickness research and mitigation initiatives

A new MRI rating scale for progressive supranuclear palsy and multiple system atrophy: validity and reliability

AIM To evaluate a standardised MRI acquisition protocol and a new image rating scale for disease severity in patients with progressive supranuclear palsy (PSP) and multiple systems atrophy (MSA) in a large multicentre study. METHODS The MRI protocol consisted of two-dimensional sagittal and axial T1, axial PD, and axial and coronal T2 weighted acquisitions. The 32 item ordinal scale evaluated abnormalities within the basal ganglia and posterior fossa, blind to diagnosis. Among 760 patients in the study population (PSP = 362, MSA = 398), 627 had per protocol images (PSP = 297, MSA = 330). Intra-rater (n = 60) and inter-rater (n = 555) reliability were assessed through Cohen's statistic, and scale structure through principal component analysis (PCA) (n = 441). Internal consistency and reliability were checked. Discriminant and predictive validity of extracted factors and total scores were tested for disease severity as per clinical diagnosis. RESULTS Intra-rater and inter-rater reliability were acceptable for 25 (78%) of the items scored (≥ 0.41). PCA revealed four meaningful clusters of covarying parameters (factor (F) F1: brainstem and cerebellum; F2: midbrain; F3: putamen; F4: other basal ganglia) with good to excellent internal consistency (Cronbach α 0.75-0.93) and moderate to excellent reliability (intraclass coefficient: F1: 0.92; F2: 0.79; F3: 0.71; F4: 0.49). The total score significantly discriminated for disease severity or diagnosis; factorial scores differentially discriminated for disease severity according to diagnosis (PSP: F1-F2; MSA: F2-F3). The total score was significantly related to survival in PSP (p<0.0007) or MSA (p<0.0005), indicating good predictive validity. CONCLUSIONS The scale is suitable for use in the context of multicentre studies and can reliably and consistently measure MRI abnormalities in PSP and MSA. Clinical Trial Registration Number The study protocol was filed in the open clinical trial registry (http://www.clinicaltrials.gov) with ID No NCT00211224